Books

Books reviewed in this article:
B ohlen , D.H. 1989. The Birds of Illinois.
B undy , G., C onnor , R.J. & H arrison , C.J.O. 1989. Birds of the Eastern Province of Saudi Arabia.
D wenger , R. 1989. Die Dohle. Pp. 148, 40 black-and-white photographs, maps.
D ymond , J.N., F raser , P.A. & G antlett , S.J.M. 1989. Rare Birds in Britain and Ireland.
Fa aborg , J. 1988. Ornithology. An ecological approach.
G ill , F.B. 1990. Ornithology.
F ord , H.A. 1989. Ecology of Birds: An Australian perspective.
G ill , F.B. 1990. Ornithology.
G onzales , P.C. & R ees , C.P. 1988. Birds of the Philippines.
G uraya , S.S. 1989. Ovarian Follicles in Reptiles and Birds.
M c I ntyre , J.W. 1988. Spirit of the Northern Lakes: the Common Loon.
N ewton , I. (ed.) 1989. Lifetime Reproduction in Birds.
O tte , D. & E ndler , J.A. 1989. Speciation and its Consequences.
O uellet , H. (ed.) 1989. Acta XIX Congressus Internationalis Ornithologici, Volumes 1 & 2.
P ennycuick , C.J. 1989. Bird Flight Performance: A practical calculation manual.
P eterjohn , B.G. 1989. The Birds of Ohio.
P range , H. 1989. Der Graue Kranich.
S icutch , A.F. 1989. Birds Asleep.
T homson , M.C. & E ly , C. 1989. Birds in Kansas
B ohlen , D.H. 1989. The Birds of Illinois.
P eterjohn , B.G. 1989. The Birds of Ohio.
Voous, K.H. 1988. Owls of the Northern Hemisphere.
V uilleumier , F. & M onasterio , M. (eds.) 1986. High Altitude Tropical Biogeography.     

Transcellular activation of the human immunodeficiency virus type 1 long terminal repeat in cocultured lymphocytes.

One of the unexplained aspects of the progression of AIDS is that immunological abnormalities are detectable before CD4+ T-helper cell depletion occurs (A.R. Gruters, F.G. Terpstra, R. De Jong, C.J.M. Van Noesel, R.A.W. Van Lier, and F. Miedema, Eur. J. Immunol. 20:1039-1044, 1990; F. Miedema, A.J. Chantal-Petit, F.G. Terpstra, J.K.M.E. Schattenkerk, F. de Wolf, B.J.M. Al, M. Roos, J.M.A. Lang, S.A. Danner, J. Goudsmit, and P.T.A. Schellekens, J. Clin. Invest. 82:1908-1914, 1988; G.M. Shearer, D.C. Bernstein, K.S. Tung, C.S. Via, R. Redfield, S.Z. Salahuddin, and R.C. Gallo, J. Immunol. 137:2514-2521, 1986). In this report, we describe a mechanism by which human immunodeficiency virus type 1 (HIV-1)-infected cells can influence neighboring HIV-1-infected T lymphocytes and uninfected T cells as well. We have examined the interaction of T-cell and macrophage cell lines that are transfected with HIV-1 DNA by using cocultured lymphocytes. The HIV-1 constructs we used lack a functional pol gene and therefore do not produce infectious virus. Cocultivation results in the transcellular activation of the HIV long terminal repeat in the cocultured T cells. This transcellular activation is evident in as little as 3 h of cocultivation, at ratios of HIV-expressing cells to target cells as low as 1:1,000, and is dependent on the Tat-responsive element. The demonstration that a small number of HIV-expressing cells can affect a large number of uninfected bystander cells in a short period of time suggests a mechanism by which global immune dysfunction can precede the high prevalence of infected cells.     

Interleukin-1 receptor antagonist competitively inhibits the binding of interleukin-1 to the type II interleukin-1 receptor.

The interleukin-1 receptor antagonist (IL-1ra) inhibits the binding of interleukin-1 (IL-1) to T-cell lines possessing the type I IL-1 receptor; evidence has been published (Carter, D. B., Deibel, M. R. J., Dunn, C. J., Tomich, C. S., Laborde, A. L., Slightom, J. L., Berger, A. E., Bienkowski, M. J., Sun, F. F., McEwan, R. N., Harris, P. K. W., Yem, A. W., Waszak, G. A., Chosay, J. G., Sieu, L. C., Hardee, M. M., Zurcher-Neely, H. A., Reardon, I. M., Heinrickson, R. L., Truesdell, S. E., Shelly, J. A., Eessalu, T. E., Taylor, B. M., and Tracey, D. E. (1990) Nature 344, 633-638; Hannum, C. H., Wilcox, C. J., Arend, W. P., Joslin, F. G., Dripps, D. J., Heimdal, P. L., Armes, L. G., Sommer, A., Eisenberg, S. P., and Thompson, R. C. (1990) Nature 343, 336-340) that IL-Ira does not bind to the type II IL-1 receptor (IL-1RtII). In this study we examined the ability of human recombinant IL-1ra to block the binding of IL-1 to the IL-1RtII on human polymorphonuclear leukocytes (PMN) and Raji human B-lymphoma cells. The binding of 125I-IL-1 beta to PMN was competively inhibited by IL-1ra. IL-1 beta was more potent in inhibiting the binding of 125I-IL-1 beta than IL-1ra. Incubating PMN with 125I-IL-1ra in the presence of increasing concentrations of IL-1 beta or IL-1ra showed that IL-1 beta was an approximately 40-fold more potent inhibitor of binding of 125I-IL-1ra than unlabeled IL-1ra. The IL-1ra was approximately 500-fold less potent in inhibiting the binding of 125I-IL-1 alpha than IL-1 alpha. IL-1ra was also able to competitively inhibit binding of 125I-IL-1 beta to Raji cells. PMN or Raji cells were also incubated with 125I-IL-1 in the absence or presence of IL-1 or IL-1ra. After cross-linking of IL-1 to cells followed by specific immunoprecipitation, sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed a band at 85 kDa corresponding to the 68-kDa IL-1RtII. However, in the presence of an excess of either unlabeled IL-1 or IL-1ra, the 85-kDa IL-1.IL-1RtII complex was not present. These findings demonstrate that the IL-1ra recognizes and blocks IL-1 binding to the IL-1RtII.     

The nucleocapsid protein of severe acute respiratory syndrome-coronavirus inhibits the activity of cyclin-cyclin-dependent kinase complex and blocks S phase progression in mammalian cells

Deregulation of the cell cycle is a common strategy employed by many DNA and RNA viruses to trap and exploit the host cell machinery toward their own benefit. In many coronaviruses, the nucleocapsid protein (N protein) has been shown to inhibit cell cycle progression although the mechanism behind this is poorly understood. The N protein of severe acute respiratory syndrome-coronavirus (SARS-CoV) bears signature motifs for binding to cyclin and phosphorylation by cyclin-dependent kinase (CDK) and has recently been reported by us to get phosphorylated by the cyclin-CDK complex (Surjit, M., Kumar, R., Mishra, R. N., Reddy, M. K., Chow, V. T., and Lal, S. K. (2005) J. Virol. 79, 11476-11486). In the present study, we prove that the N protein of SARS-CoV can inhibit S phase progression in mammalian cell lines. N protein expression was found to directly inhibit the activity of the cyclin-CDK complex, resulting in hypophosphorylation of retinoblastoma protein with a concomitant down-regulation in E2F1-mediated transactivation. Coexpression of E2F1 under such conditions could restore the expression of S phase genes. Analysis of RXL and CDK phosphorylation mutant N protein identified the mechanism of inhibition of CDK4 and CDK2 activity to be different. Whereas N protein could directly bind to cyclin D and inhibit the activity of CDK4-cyclin D complex; inhibition of CDK2 activity appeared to be achieved in two different ways: indirectly by down-regulation of protein levels of CDK2, cyclin E, and cyclin A and by direct binding of N protein to CDK2-cyclin complex. Down-regulation of E2F1 targets was also observed in SARS-CoV-infected VeroE6 cells. These data suggest that the S phase inhibitory activity of the N protein may have major significance during viral pathogenesis.     

Biphasic activation of two mitogen-activated protein kinases during the cell cycle in mammalian cells.

We studied mitogen-activated protein kinase (MAPK) activities during the cell cycle of Chinese hamster ovary (CHO) cells using site-specific antibodies against extracellular signal-regulated kinase-1, a 44-kDa MAPK (Boulton, T.G., Yancopoulos, G.D., Gregory, J.S., Slauer, C., Moomaw, C., Hsu, J., and Cobb, M.H. (1990) Science 249, 64-67). These antibodies detected two distinct MAPKs (44- and 42-kDa MAPKs) in CHO cells. CHO cells were arrested at metaphase in the M phase by treatment with nocodazole, and activities of MAPKs were analyzed at specific time points after release from arrest. Immune complex kinase assay and renaturation and phosphorylation assay in substrate-containing gel revealed that both 44- and 42-kDa MAPKs had activities in the G1 through S and G2/M phases and were activated biphasically, in the G1 phase and around the M phase. MAPKs were inactivated in metaphase-arrested cells. The amount of MAPKs did not change significantly in the cell cycle. In the G1, S, and G2/M phases, MAPKs were phosphorylated on both tyrosine and threonine residues and dephosphorylated in metaphase-arrested cells. Our data suggest that MAPKs may play some role in the cell cycle other than G0/G1 transition.     

Reviews

Plant Lectins. By A. P ustzai .
Techniques for the Rapid Detection of Plant Pathogens . Ed. by J. M. D uncan and L. T orrance .
Ecological Genetics and Air Pollution. Ed. by G. R. T aylor , Jr., L. F. P itelka and M. T. C legg .
Arctic Ecosystems in a Changing Climate. Ed. By F. S. C hapin III, R. L. J efferies , J. F. R eynolds , G. R. S haver , J. S voboda and E. W. C hu .     

Books

Books reviewed in this article:
B aker . K. 1993. Identification Guide to European Non-passerines.
B arnard . C., G ilbert , F. & M c G regor
B askett , T.S., S ayre . M.W., T omlinson , R.E. & M irarchi .
B ezzel . E. 1993. Kompendium der Vögel Mitteleuropas.
B right , M. 1993. The Private Life of Birds.
C ook , M. 1992. The Birds of Moray and Nairn.
D avison . G.W.H. 1992. Birds of Mount Kinabalu. Borneo.
E rritzoe . J. 1993. The Buds of CITES and How to Identify Them.
F arner , D.S., K ing , J.R. & P arkes , K.C.
G ibbons , D.W., R eid , J.B. & C hapman . R.A. (eds). 1993. The New Atlas of Breeding Birds in Britain and Ireland.
H illman , J.C.
H uxley . E.
J ackson . C.E. 1993. Great Bird Paintings of the World.
J ohnsgard . P.A. 1993. Cormorants, Darters and Pelicans of the World.
M adge . S. & B urn , H. 1994. Crows and Jays. A Guide to the Crows, Jays and Magpies of the World.
N icolai . B. (ed.).
P ower , D.M. (ed.).
P riklonskiy . S.G. (ed.).
R alph . R. 1993. William MacGillivray.
R obinson , D. & C hapman , A.
S harp . P.J. 1993. Avian Endocrinology.
S mith , K.W., D fe , C.W., F earnside . J.D., F letcher , E.W. & S mith , R.N.
S olomon . D. & W illiams , J.
S ørensen , S., B loch . D. & L angvad . S.
Z immerman , J.L.     

The hereditary hemochromatosis protein, HFE, specifically regulates transferrin-mediated iron uptake in HeLa cells

HFE is the protein product of the gene mutated in the autosomal recessive disease hereditary hemochromatosis (Feder, J. N., Gnirke, A., Thomas, W., Tsuchihashi, Z., Ruddy, D. A., Basava, A., Dormishian, F., Domingo, R. J., Ellis, M. C., Fullan, A., Hinton, L. M., Jones, N. L., Kimmel, B. E., Kronmal, G. S., Lauer, P., Lee, V. K., Loeb, D. B., Mapa, F. A., McClelland, E., Meyer, N. C., Mintier, G. A., Moeller, N., Moore, T., Morikang, E., Prasss, C. E., Quintana, L., Starnes, S. M., Schatzman, R. C., Brunke, K. J., Drayna, D. T., Risch, N. J., Bacon, B. R., and Wolff, R. R. (1996) Nat. Genet. 13, 399-408). At the cell surface, HFE complexes with transferrin receptor (TfR), increasing the dissociation constant of transferrin (Tf) for its receptor 10-fold (Gross, C. N., Irrinki, A., Feder, J. N., and Enns, C. A. (1998) J. Biol. Chem. 273, 22068-22074; Feder, J. N., Penny, D. M., Irrinki, A., Lee, V. K., Lebron, J. A., Watson, N. , Tsuchihashi, Z., Sigal, E., Bjorkman, P. J., and Schatzman, R. C. (1998) Proc. Natl. Acad. Sci. U S A 95, 1472-1477). HFE does not remain at the cell surface, but traffics with TfR to Tf-positive internal compartments (Gross et al., 1998). Using a HeLa cell line in which the expression of HFE is controlled by tetracycline, we show that the expression of HFE reduces 55Fe uptake from Tf by 33% but does not affect the endocytic or exocytic rates of TfR cycling. Therefore, HFE appears to reduce cellular acquisition of iron from Tf within endocytic compartments. HFE specifically reduces iron uptake from Tf, as non-Tf-mediated iron uptake from Fe-nitrilotriacetic acid is not altered. These results explain the decreased ferritin levels seen in our HeLa cell system and demonstrate the specific control of HFE over the Tf-mediated pathway of iron uptake. These results also have implications for the understanding of cellular iron homeostasis in organs such as the liver, pancreas, heart, and spleen that are iron loaded in hereditary hemochromatotic individuals lacking functional HFE.     

Books

Books reviewed in this article: Antas , P.T.Z. & Cavalcanti , R.B. 1988. Aves Comuns do Planalto Central. Chandler , R.J. 1989. The Macmillan Field Guide to North Atlantic Shorebirds. Clutton -Brock , T.H. (ed.). 1988. Reproductive Success: studies of individual variations in contrasting breeding systems. Delin , H. & Svensson , L. 1988. Photographic Guide to the Birds of Britain and Europe. Dunning , J.S. 1987. South American Birds—a photographic aid to identification. Ewans , M. 1989. Bharatpur Bird Paradise. Frugis , S., Malaguzzi , G., Vicini , G. & Cristina , Grimmett , R.F.A. & Jones , T.A. (eds) 1989. Important Bird Areas in Europe. Hutchinson , C.D. 1989. Birds in Ireland. Iapichino , C. & Massa , B. 1989. The Birds of Sicily. Kilham , L. 1989. The American Crow and the Common Raven. Kooyman , G.L. 1989. Diverse Divers: physiology and behaviour. Mearns , B. & Mearns , R. 1988. Biographies for Birdwatchers Mingozzi , T., Boano , G., Pulcher , C. & Collaborators. Poole , A. 1989. Ospreys: a Natural and Unnatural History. Pringle , J.D. 1987. The Shorebirds of Australia. Rheinwald , G., Ogden , J. & Schulz , H. (eds) 1989. Weißstorch: Status und Schutz. White Stork: Status and Conservation. Roughgarden , J., May , R.M. & Levin S.A. 1989. Perspectives in Ecological Theory. Sheail , J. 1985. Pesticides and Nature Conservation—The British Experience 1950–1975. Stalmaster , M. 1987. The Bald Eagle. Turner , A. & Rose , C. 1989. A Handbook to the Swallows and Martins of the World. Viksne , J. (ed.) 1989. Latvian Breeding Bird Atlas 1980–1984 (in Latvian, Russian and English). Ashmole , M. & P. 1989. Natural History Excursions in Tenerife. Axelson , R.D. 1989. Caring for Your Pet Bird. Bauer , K. 1989. Rote Listen der Gefährdeten Vögel und Säugetiere Österreichs und Verzeichnisse der in Österreich vorkommenden Arten. Bircham , P. 1989. The Birds of Cambridgeshire Boyd , H. & Pirot , J.-Y. (eds) 1989. Flyways and Reserve Networks for Waterbirds. Brasseler , H. 1987. Bibliography of Ornithological Bibliographies II. Donkin , R.A. 1989. The Muscovy Duck Cairina moschata domestica. Elliott , R.E. 1989. Birds of Islay. Flint , V.E., Boehme , R.L., Kostin , Y.V. & Kuznetsov , A.A. 1989. A Field Guide to the Birds of the USSR. Translated from the Russian by N. Bourso-Leland. Holmgren , V.C. 1986. The Way of the Hummingbird. Hulm , P. (ed.) 1989. World Wildlife Conservation Yearbook 1987/88. Inskipp , T., Broad , S. & Luxmoore , R. (eds) 1988. Significant Trade in Wildlife: A review of the Selected Species in CITES Appendix II. Volume 3: Birds Kofalk , H. 1989. No Woman Tenderfoot. Florence Merriam Bailey, Pioneer Naturalist. Kondratiev , A. Ya. 1989. Bulletin of the Working Group on Waders (in Russian). Lohmann , M. & Haarmann , K. 1989. Vogelparadiese—122 Biotope zwischen Wattenmeer und Bodensee. Lorand , S. & Atkin , K. 1989. The Birds of Lincolnshire and South Humberside. Monval , J.-Y. & Pirot , J.-Y. (rds) 1989. Results of the IWRB International Waterfowl Census 1967–1986. Moss , S. 1988. Natural History of the Antarctic Peninsula. Ogilvie , M. & Winter , S. (eds) 1989. Best Days with British Birds. Orton , D.A. 1989. The Hawkwatcher. Adventures among birds of prey in the wild. Paynter , R.A. Jr. 1989. Ornithological Gazetteer of Paraguay. 2nd ed. Pemberton , J.E. (ed.) 1989. The Birdwatcher's Yearbook and Diary 1990. Pickford , P. & B., & Tarboton , W. 1989. African Birds of Prey. Reilly , P. 1988. The Lyrebird. Santa Barbara Software Products 1988. World Birdbase: Users Manual. Santa Barbara: Santa Barbara Software Products. Schembri , P.J. & Sultana , J. (ed.) 1989. Red Data Book for the Maltese Islands. Scottish Chouch Study Group . 1989. Choughs and Land-use in Europe. Van Someren , G.R. Cunningham & Van Someren , L.A. 1989. Van Somerens' Birds I.     

Chk1 mediates S and G2 arrests through Cdc25A degradation in response to DNA-damaging agents

UV and ionizing radiation (IR) activate DNA damage checkpoints and induce Cdc25A degradation (Mailand, N., Falck, J., Lukas, C., Syljuasen, R. G., Welcker, M., Bartek, J., and Lukas, J. (2000) Science 288, 1425-1429; Falck, J., Mailand, N., Syljuasen, R. G., Bartek, J., and Lukas J. (2001) Nature 410, 842-847). The degradation of Cdc25A is abrogated by caffeine, which implicates Chk1 as the potential mediator (Mailand, N., Falck, J., Lukas, C., Syljuasen, R. G., Welcker, M., Bartek, J., and Lukas, J. (2000) Science 288, 1425-1429). However, the involvement of Chk1 is far from clear, because caffeine is a rather nonspecific inhibitor of the ATR/Chk1 signaling pathway. Additionally, it is not known whether DNA-damaging drugs commonly used in chemotherapy, which may activate different signal transduction pathways than UV or IR, also confer Cdc25A degradation. Herein, we show that camptothecin and doxorubicin, two widely used topoisomerase inhibitors conferring S and G2 arrest, respectively, cause the degradation of Cdc25A. Using a small interfering RNA that enables the specific elimination of Chk1 expression, we show that the observed proteolysis of Cdc25A is mediated through Chk1. Moreover, Cdc25A overexpression abrogates the Chk1-mediated degradation and overcomes the doxorubicin-induced G2 arrest through dephosphorylation and activation of Cdc2/Cdk1 in a dose-dependent manner. These results suggest that: (a) Cdc25A is involved in the G2/M transition in addition to its commonly accepted effect on G1/S progression, and (b) Chk1 mediates both S and G2 checkpoint and is thus a more ubiquitous cell cycle checkpoint mediator than previously thought.     

Heparin suppresses specific second messenger pathways for protooncogene expression in rat vascular smooth muscle cells.

We investigated the molecular mechanisms underlying the ability of heparin to inhibit vascular smooth muscle cell (VSMC) growth. Previous experiments have shown that heparin inhibits induction of c-fos and c-myc protooncogene mRNA in rat VSMC stimulated by phorbol 12-myristate 13-acetate (PMA) but not when stimulated by epidermal growth factor (EGF) (Pukac, L. A., Castellot, J. J., Wright, T. C., Caleb, B. L., and Karnovsky, M. J. (1990) Cell Regul. 1, 435-443). The present experiments show that these mitogens activate distinct second messenger pathways in VSMC, because PMA but not EGF induction of c-fos and c-myc mRNA was suppressed in protein kinase C (PKC) down-regulated VSMC; this suggests that EGF does not act through a PKC-dependent pathway for induction of these genes. Heparin inhibited serum stimulation of c-fos mRNA in control VSMC, but heparin did not inhibit the smaller but significant serum stimulation of c-fos mRNA in PKC down-regulated VSMC, indicating that heparin may selectively inhibit PKC-dependent, but not PKC-independent, stimulation of gene expression. To further determine if heparin inhibits non-PKC pathways, VSMC were treated with dibutyryl cAMP, 3-isobutyl-1-methyl-xanthine, and Ca2+ ionophore A23187; stimulation of c-fos mRNA by this treatment was not inhibited by heparin. DNA synthesis and cell proliferation were inhibited in rat VSMC exposed briefly to heparin during the G0/G1 phase of the cell cycle. These experiments indicate heparin can act early in the cell cycle and suggest PKC-dependent but not PKC-independent signaling pathways for gene expression are selectively sensitive to heparin inhibition.     

A small molecule inhibitor of isoprenylcysteine carboxymethyltransferase induces autophagic cell death in PC3 prostate cancer cells

A number of proteins involved in cell growth control, including members of the Ras family of GTPases, are modified at their C terminus by a three-step posttranslational process termed prenylation. The enzyme isoprenylcysteine carboxylmethyl-transferase (Icmt) catalyzes the last step in this process, and genetic and pharmacological suppression of Icmt activity significantly impacts on cell growth and oncogenesis. Screening of a diverse chemical library led to the identification of a specific small molecule inhibitor of Icmt, cysmethynil, that inhibited growth factor signaling and tumorigenesis in an in vitro cancer cell model (Winter-Vann, A. M., Baron, R. A., Wong, W., dela Cruz, J., York, J. D., Gooden, D. M., Bergo, M. O., Young, S. G., Toone, E. J., and Casey, P. J. (2005) Proc. Natl. Acad. Sci. U. S. A. 102, 4336-4341). To further evaluate the mechanisms through which this Icmt inhibitor impacts on cancer cells, we developed both in vitro and in vivo models utilizing PC3 prostate cancer cells. Treatment of these cells with cysmethynil resulted in both an accumulation of cells in the G(1) phase and cell death. Treatment of mice harboring PC3 cell-derived xenograft tumors with cysmethynil resulted in markedly reduced tumor size. Analysis of cell death pathways unexpectedly showed minimal impact of cysmethynil treatment on apoptosis; rather, drug treatment significantly enhanced autophagy and autophagic cell death. Cysmethynil-treated cells displayed reduced mammalian target of rapamycin (mTOR) signaling, providing a potential mechanism for the excessive autophagy as well as G(1) cell cycle arrest observed. These results identify a novel mechanism for the antitumor activity of Icmt inhibition. Further, the dual effects of cell death and cell cycle arrest by cysmethynil treatment strengthen the rationale for targeting Icmt in cancer chemotherapy.     

Books

Book reviewed in this article:
B eehler , B.M. 1991. A Naturalist in New Guinea
B erthold , P. 1990. Vogelzug: eine kurze. aktuelle Gesamtübersicht
B ezzel , E. & P rinzinger , R. 1990. Ornithologie
B ub , H. 1991. Bird Trapping and Bird Banding
B urger , J. (ed.). 1988
B urke , T., D olf , G., J effreys , A.J. & W olff , R. (eds) 1991. DNA Fingerprinting: approaches and applications
C roxall , J.P. (ed.). 1991. Seabird Status and Conservation: a supplement
E rard , C. 1990. Ecologie et Comportement de Gobe-mouches
G alati , R. 1991. Golden-crowned Kinglets, Treetop Nesters of the North Woods
J ohnsgard , P.A. 1988. North American Owls: biology and natural history
J ohnsgard , P.A. 1991. Bustards. Hemipodes, and Sandgrouse: birds of dry places
K uroda , N. 1990. The Jungle Crows of Tokyo
L ekagul , B. & R ound , P.D. 1991. Birds of Thailand
L loyd , C. T asker , M.L. & P artridge , K. 1991. The Status of Seabirds in Britain and Ireland
L örhl , H. 1991. Die Haubenmeise
L oye , J. E. & Z uk , M. (eds) 1991. Bird-Parasite Interactions: ecology, evolution and behaviour
M itchell , A. 1989. The Fragile South Pacific: an ecological odyssey
O lney , P.J.S. & E llis , P. (eds) 1990. International Zoo Yearbook 1989, Vol. 29
O wen , M. & B lack , J.M. 1990. Waterfowl Ecology
R oberts , T.J. 1991. The Birds of Pakistan. Vol. 1; Regional studies and non-passeriformes
S chonn S., S cherzinger W., E xo K-L. & I lle R. 1991. Der Steinkauz. Athene noctua. Pp. 235, 139 monochrome photographs, 28 tables & 2 colour plates
S ibley , C.C. & A hlquist , J.E. 1990. Phylogeny and Classification of Birds: a study in molecular evolution
S kutch , A.F. 1991. Life of the Pigeon
S troud , D. & G lue , D. 1991. Britain's Birds in 1989–90: The conservation and monitoring review
Y eatman -B ekthelot , D. 1991. Atlas des Oiseaux de France en Hiver.     

Isolation of BamHI variants with reduced cleavage activities

Derivation of the bamhIR sequence (Brooks, J. E., Nathan, P.D., Landry, D., Sznyter, L.A., Waite-Rees, P., Ives, C. C., Mazzola, L. M., Slatko, B. E., and Benner, J. S. (1991) Nucleic Acids Res., in press), the gene coding for BamHI endonuclease, has facilitated construction of an Escherichia coli strain that overproduces BamHI endonuclease (W. E. Jack, L. Greenough, L. F. Dorner, S. Y. Xu, T. Strezelecka, A. K. Aggarwal, and I. Schildkraut, submitted for publication). As expected, low-level constitutive expression of the bamhIR gene in E. coli from the Ptac promotor construct is lethal to the host unless the bamHIM gene, which encodes the BamHI methylase, is also expressed within the cell. We identified four classes of BamHI endonuclease variants deficient in catalysis by selecting for survival of a host deficient for bamHIM gene, transformed with mutagenized copies of the bamhIR gene, and then screening the surviving cell extracts for DNA cleavage and binding activities. Class I variants (G56S, G91S/T153I, T114I, G130R, E135K, T153I, T157I, G194D) displayed 0.1-1% of the wild-type cleavage activity; class II variant (D94N) lacked cleavage activity but retained wild-type DNA binding specificity; class III variants (E77K, E113K) lacked cleavage activity but bound DNA more tightly; class IV variants (G56D, G90D, G91S, R122H, R155H) lacked both binding and cleavage activities. Variants with residual cleavage activities induced the E. coli SOS response and thus are presumed to cleave chromosomal DNA in vivo. We conclude that Glu77, Asp94, and Glu113 residues are essential for BamHI catalytic function.     

Confirmation of the expression of a large set of conserved hypothetical proteins in Shewanella oneidensis MR-1

High-throughput "omic" technologies have allowed for a relatively rapid, yet comprehensive analysis of the global expression patterns within an organism in response to perturbations. In the current study, 9503 different tryptic peptides were identified with high confidence from capillary liquid chromatography-mass spectrometry analysis of 26 chemostat cultures of Shewanella oneidensis MR-1 under various conditions. Using at least one distinctive and a total of two total peptide identifications per protein, we detected the expression of 758 conserved hypothetical proteins. This included 359 such proteins previously described [Kolker, E., Picone, A.F., Galperin, M.Y., Romine, M.F., Higdon, R., Makarova, K.S., Kolker, N., Anderson, G.A., Qiu, X., Auberry, K.J., Babnigg, G., Beliaev, A.S., Edlefsen, P., Elias, D.A., Gorby, Y.A., Holzman, T., Klappenbach, J.A., Konstantinidis, K.T., Land, M.L., Lipton, M.S., McCue, L.A., Monroe, M., Pasa-Tolic, L., Pinchuk, G., Purvine, S., Serres, M.H., Tsapin, S., Zakrajsek, B.A., Zhu, W., Zhou, J., Larimer, F.W., Lawrence, C.E., Riley, M., Collart, F.R., Yates, J.R., III, Smith, R.D., Giometti, C.S., Nealson, K.H., Fredrickson, J.K., Tiedje, J.M., 2005. Global profiling of Shewanella oneidensis MR-1: expression of hypothetical genes and improved functional annotations. Proc Natl Acad Sci U S A 102, 2099-2104] with an additional 399 reported herein for the first time. The latter 399 proteins ranged from 5.3 to 208.3 kDa, with 44 being of 100 amino acid residues or less. Using a combination of information including peptide detection in cells grown under specific culture conditions and predictive algorithms such as PSORT and PSORT-B, possible/plausible functions are proposed for some conserved hypothetical proteins. Such proteins were found not only to be expressed, but 19 were only expressed under certain culturing conditions, thereby providing insight into potential functions. These findings also impact the genomic annotation for S. oneidensis MR-1 by confirming that these genes code for expressed proteins. Our results indicate that 399 proteins can now be upgraded from "conserved hypothetical protein" to "expressed protein in Shewanella," 19 of which appeared to be expressed under specific culture conditions.     

Phospholipase C-delta1 expression is linked to proliferation, DNA synthesis, and cyclin E levels

We previously reported that phospholipase C-delta1 (PLC-delta1) accumulates in the nucleus at the G1/S transition, which is largely dependent on its binding to phosphatidylinositol 4,5-bisphosphate ( Stallings, J. D., Tall, E. G., Pentyala, S., and Rebecchi, M. J. (2005) J. Biol. Chem. 280, 22060-22069 ). Here, using small interfering RNA (siRNA) that specifically targets rat PLC-delta1, we investigated whether this enzyme plays a role in cell cycle control. Inhibiting expression of PLC-delta1 significantly decreased proliferation of rat C6 glioma cells and altered S phase progression. [3H]Thymidine labeling and fluorescence-activated cell sorting analysis indicated that the rates of G1/S transition and DNA synthesis were enhanced. On the other hand, knockdown cultures released from the G1/S boundary were slower to reach full G2/M DNA content, consistent with a delay in S phase. The levels of cyclin E, a key regulator of the G1/S transition and DNA synthesis, were elevated in asynchronous cultures as well as those blocked at the G1/S boundary. Epifluorescence imaging showed that transient expression of human phospholipase C-delta1, resistant to these siRNA, suppressed expression of cyclin E at the G1/S boundary despite treatment of cultures with rat-specific siRNA. Although whole cell levels of phosphatidylinositol 4,5-bisphosphate were unchanged, suppression of PLC-delta1 led to a significant rise in the nuclear levels of this phospholipid at the G1/S boundary. These results support a role for PLC-delta1 and nuclear phospholipid metabolism in regulating cell cycle progression.     

Identification of a uniquely immunodominant, cross-reacting site in the human immunodeficiency virus endonuclease protein.

One of the features of the life cycle of retroviruses is insertion of the proviral DNA into host chromosomes. A protein encoded by the 3' end of the pol gene of the virus genome has been shown to possess endonuclease activity (D. P. Grandgenett, A. C. Vora, and R. D. Schiff, Virology 89:119-132, 1978), which is necessary for DNA integration. Sera from the majority of human immunodeficiency virus (HIV)-infected individuals react with endonuclease protein p31 in serological tests (J. S. Allan, J. E. Coligan, T.-H. Lee, F. Barin, P. J. Kanki, S. M'Boup, M. F. McLane, J. E. Groopman, and M. Essex, Blood 69:331-333, 1987; E. F. Lillehoj, F. H. R. Salazar, R. J. Mervis, M. G. Raum, H. W. Chan, N. Ahmad, and S. Venkatesan, J. Virol. 62:3053-3058, 1988; K. S. Steimer, K. W. Higgins, M. A. Powers, J. C. Stephans, A. Gyenes, G. George-Nascimento, P. A. Liciw, P. J. Barr, R. A. Hallewell, and R. Sanchez-Pescador, J. Virol. 58:9-16, 1986). It is not known, however, which part of the protein represents the target(s) for antibody response. To study this, we synthesized peptides and used them in an enzyme-linked immunosorbent assay system to map the reactivity of human immunodeficiency virus type 1 (HIV-1) antibody-positive sera to the different regions of the HIV endonuclease. A uniquely antigenic, HIV-1- and HIV-2-cross-reacting site was identified in the central part of this protein from Phe-663 to Trp-670.